Background

Proteinuria in dogs with kidney disease can contribute to protein-energy wasting and malnutrition. Little is known about amino acid (AA) status in dogs with protein-losing nephropathy (PLN).

Objectives

The purpose of our study was to further elucidate AA status in PLN dogs, with the hypothesis that PLN dogs would have altered AA status as compared to healthy dogs.

Animals

Thirty client-owned PLN dogs were compared to 10 healthy control dogs.

Methods

Prospective observational study. Dogs with PLN that were presented to the teaching hospital were enrolled. Plasma AA profiles were measured using an automated high-performance liquid chromatography AA analyzer.

Results

Compared to control dogs, PLN dogs had significantly lower concentrations of leucine, threonine, histidine, glycine, proline, asparagine, tyrosine, o-hydroxyproline, and serine, as well as sums of both essential and nonessential AA (P < .05). Dogs with PLN had significantly lower ratios of tyrosine-to-phenylalanine and glycine-to-serine (P < .05), and a significantly greater ratio of valine-to-glycine (P < .05).

Conclusions and clinical importance

Dogs with PLN have altered AA status compared to healthy dogs. These findings could have therapeutic implications in determining optimal management of PLN dogs, such as providing AA supplementation along with other standard treatment.

Background

Chronic kidney disease (CKD) leads to low serum concentrations of vitamin D metabolites. Thus, hypovitaminosis D associated with CKD might contribute to disease progression via increased concentration of renin angiotensin aldosterone system (RAAS) mediators.

Objectives

To evaluate whether supplementation with calcifediol affects equilibrium concentrations of selected mediators of the RAAS. We hypothesized that vitamin D supplementation will decrease concentration of circulating RAAS mediators in dogs with CKD.

Animals

Six client-owned adult dogs with IRIS Stage 2 and 3 CKD.

Methods

Prospective study. Serum 25-hydroxyvitamin D (25[OH]D), 1,25-dihydroxyvitamin D (1,25[OH]₂ D), 24,25-dihydroxyvitamin D (24,25[OH]₂ D), RAAS mediators (angiotensin I/II/III/IV/1-5/1-7, and aldosterone), and surrogate angiotensin converting enzyme (ACE) activity (calculated by the ratio of angiotensin II to angiotensin I) were evaluated at baseline, after 3 months of calcifediol supplementation, and 2 months after discontinuing administration of supplement.

Results

All serum vitamin D metabolite concentrations increased significantly by month 3 (P < .001): 25(OH)D (median 250 ng/mL; range, 204-310), compared to baseline (median 43.2 ng/mL; range, 33.8-58.3 ng/mL); 1,25(OH)₂ D (median 66.1 pg/mL; range, 57.3-88.1 pg/mL) compared to baseline (median 35.2 pg/mL; range, 29.3-56.7 pg/mL); 24,25(OH)₂ D (median 68.4 ng/mL; range, 22.1-142.0 ng/mL) compared to baseline (median 14.4 ng/mL; range, 9.0-21.3 ng/mL). Calculated ACE activity was significantly lower at month 3 (median 0.5; range, 0.4-1.0) compared to baseline (median 0.7; range, 0.6-1.3; P = .01). There were no significant differences in any of the evaluated RAAS variables at any other time-point.

Conclusions and clinical importance

Short-term calcifediol supplementation in this small group of CKD dogs appeared to decrease ACE activity.